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The Palaeogene Slieve Gullion Igneous Centre in southern Armagh, Northern Ireland, consists of a layered central intrusive complex surrounded by a prominent and slightly older ring-dyke that intrudes both Lower Palaeozoic sedimentary rocks and the Caledonian Newry Granodiorite pluton (452 Ma). The ring-dyke comprises two major rock types: porphyritic felsite and porphyritic granophyre. We analysed both ring-dyke lithologies, both types of country rock, and a local Palaeogene basalt dyke sample for Sr and Nd isotopes. Trace element and whole rock data for this suite suggest that there are two distinct groups of both felsite and granophyre: one Si-rich and one Si-poor, most likely representing two magmas from a zoned chamber and their mushy chamber wall equivalents (McDonnell et al. 2004). Isotope data show the low-Si rocks to be higher in radiogenic Sr than the high-Si rocks, which is inconsistent with a simple AFC-scenario of increasing sediment assimilation with higher degrees of differentiation. However, using MORB-type basalt as a starting composition, the low-Si ring-dyke rocks can be modelled through AFC with Lower Palaeozoic sedimentary rock as the contaminant. The decreasing 87Sr/86Sr trend from low-Si to high-Si dyke rocks, in turn, represents a second stage of contamination. Selective assimilation of the most fusible portions of Newry Granodiorite, which is lower in radiogenic Sr than the local sedimentary rocks, appears to be the most plausible solution. The Sr and Nd data are consistent with (a) at least a two-stage contamination history during upper crustal residence and storage, whereby fractionating magmas of basaltic and intermediate composition are contaminated by local sedimentary rocks, giving rise to rhyolite magmas that experience additional shallow contamination by Newry Granodiorite, and (b) a zoned rhyolite magma chamber where high-Si magma is stored in the upper part of the chamber where crystallization and crustal contamination are most extensive.

Cerebral palsy (CP) can occur in term infants with or without preceding newborn encephalopathy. We compared the type and severity of CP and associated disability in these two groups. Participants from a population-based case-control study of term newborn encephalopathy were followed up for 6 years and linked to the Western Australian Cerebral Palsy Register. The remaining term infants with CP for the same period were also identified from the Cerebral Palsy Register. 13% of neonatal survivors of term newborn encephalopathy had CP, a rate of 116 per 1000 term live births. Overall, 24% of term infants with CP followed newborn encephalopathy. CP following newborn encephalopathy was more likely to: affect males (72% vs 56%); be severe (47% vs 25%); and be of spastic quadriplegia or dyskinetic types. Cognitive impairment was more common (75% vs 43%) and severe (41% vs 16%), as was epilepsy (53% vs 29%) in survivors of encephalopathy. These children were also more likely to: be non-verbal (47% vs 22%); have a severe composite disability score (47% vs 26%); and die between time of diagnosis of CP and age 6 years (5-year cumulative mortality 19% vs 5%). Children born at term who develop CP following newborn encephalopathy have a poorer prognosis than those with CP who were not encephalopathic in the first week of life.

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